Stabilisasi Resp & Hemidinamik

8/10/2019 Stabilisasi Resp & Hemidinamik

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Stabilisasi Respirasi

dan Hemodinamik sertaPemilihan Anestesi

(Anesthesia for the Trauma patient)

Tatang Bisri

Bag/SMF Anestesiologi & Reanimasi

FK UNPAD/RS Dr. Hasan Sadikin-Bandung


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Trauma

USA : 1/3 off all hospital admissions directly

related to trauma.

50% of trauma deaths occurs immediately withanother 30% occurring within a few hours of

injury.

Role of anesthesiologist: primary resuscitator,

providing anesthesia because many traumavictims require immediate surgery.


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Trauma (2)

Remember : drugs abuse, acutelyintoxicated, carriers of hepatitis or HIV.

Assume all multiple trauma patients havea cervical spine injury, a full stomach andare hypovolemic.

All patients should have initial stabilizationof the cervical spine before any airwaymanipulation.


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RAPID OVERVIEW

( Differentiation between stable, unstable and dead or dying patient )

PRIMARY SURVEY

( Evaluation and Concurrent Resuscitation )

1) Airway

2) Breathing

3) Circulation

4) Neurologic Function

5) Examination of undressed patient

( Essential Laboratory and Radiologic Examination )

SECONDARY SURVEY

( Detailed and Systematic Evaluation of Injury to each AnatomicRegion and Resuscitation at any time, if necessary )

Operating Room for

Emergency Surgery

Radiology Suite For Special X-rays

(CT Scan, arteriogram, esophagram)

Observation in ER

Or ICU

Operating Room


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Airway

Since hypoxemia an immediate threat to thetrauma patientmust focus on the airway.

Assume a cervical spine injury in any patientwith multisystem trauma, especially an alteredlevel of consciousness or a blunt injury abovethe clavicle.

A major trauma patients with unconsciousnessis always considered to be at increased risk foraspirationairway must be secured ASAPtracheal intubation / tracheostomy.


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Airway..(2)

Neck hyperextension and excessive axial

traction must be avoided .

During mask ventilation andlaryngoscopydemonstrated neck

movement stabilization (sand-bag,

forehead tape, rigid cervical collar ).


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Patient may require intubation

The awake patient: awake nasal ororotracheal intubation, blind nasal

intubation, rapid sequence intubation,awake tracheostomy.

The combative patient: rapid sequenceinduction.

The unconsciousness patient

The intubated patient.


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Indication definitive airway:nasotracheal, orotracheal, surgical airway

Apnea

Inability to maintain a patent airway by othermean.

Protection from aspiration of blood or vomitus.

Impending or potential compromise of theairway.

Closed head injury (GCS


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Intubation criteria:

GCS < 8

respiration irreguler

resp rate < 10 or > 40 per minute

tidal volume < 3,5 ml / kg BW

vital capacity < 15 ml / kg BW

PaO2< 70 mmHg

PaCO2> 50 mmHg

Sperry RJ et al : Manual of Neuroanesthesia, 1989.


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GCS Hemodynamic Hypnotic Urgency Neuromuscular

Stability Blocker

Yes Lidocaine 1,5 mg/kg

3 - 8 Yes Sux 1.0 mg/kg

No

Thiopental 2-3 mg/kg or

Yes propofol 1-2 mg/kg Yes Sux 1.0 mg/kg

9 - 12 + lidocaine 1,5 mg/kg No Vec 1.02 mg/kg

No Etomidate 1-2 mg/kg Yes Sux 1.0 mg/kg

Thiopental 3-4 mg/kg or

Yes propofol 1,5-2,0 mg/kg Yes Sux 1.0 mg/kg13 - 15 + lidocaine 1,5 mg/kg No Vec 0.02 mg/kg

No Etomidate 1-2 mg/kg Yes Sux 1.0 mg/kg

Lam A.M. : Anaesthetic management of acute head injury, 1995

Table : Suggested Choice for Intubation

Sux = succinylcholine ; Vec = vecuronium ; GCS = Glasgow Coma Scale


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Breathing

Most critically ill trauma patients require assistedor controlled ventilation.

Bag-valve device usually provide adequateventilation immediately after intubation andduring transportation.

O2 100%

Ventilation may be compromised bypneumothorax, flail chest, obstruction of ETT,direct pulmonary injury.


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Indication for mechanical ventilation

in patients with flail chest

Clinical evidence of respiratory failure

RR> 35 breath/min

PaO2 < 60 mmHg

PaCO2 > 55 mmHg

Vital capacity < 15 ml/kg

Clinical evidence of shock

Associated severe head injury with need tohyperventilate patients lung

Airway obstruction

Significant pre-existing chronic pulmonary

disease.


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shock

First step: recognized its present. Shock isinadequate organ perfusion and tissueoxygenation (tachycardia, peripheral

vasoconstriction cool)

Second step: identify the probable cause of theshock.

Hemorrhagic shockNon hemorrhagic shock (cardiogenic,

tension pneumothorax, neurogenic,

septic)


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Cause of hypotension in the initial

phase of trauma

Hemorrhage or extensive tissue injury

Tachycardia, narrow pulse pressure, peripheral

vasoconstriction.Th/: Crystalloid solution initially and transfuse if

2000 ml in 15 minutes does not improve BP.

Cardiac tamponadeTachycardia, dilated neck veins, muffed heart

sound.

Th/: Pericardiocentesis


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phase of trauma

Myocardial contusion

Tachycardia, cardiac dysrythmias

Th/: Crystalloid , vasodilators, inotropesPneumothorax or hemothorax

Tachycardia, dilated neck veins, absent breath

sound, dyspnoe, subcutaneus emphysemaTh/: Chest tube


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phase of trauma

Spinal cord injury

hypotension without tachycardia, narrow pulse

pressure or vasoconstriction.Th/: Crystalloid , vasopressor, inotropes.

Sepsis

Depelops typically a few hour after colon injury(in normovolemic patients manifest as modest

tachycardia, wide pulse pressure, fever)

Th/: Antibiotics, crystalloid, inotropes.


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Clinical classification of shock

Blood volume loss Clinical manifestations

Mild (40%) Agitation, confusion, or obtundation.

Supine hypotension and tachycardia.

Rapid and deep respiration


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ATLS classification of hemorrhagic shock

Class I Class II Clas III Class IV

Blood loss (ml)

Blood loss (% of BV)

Heart rate

SBP

Pulse pressure

Capillary refill test

Resp rate

Urine output

Mental status

Fluid replacement

Up to 750

Up to 15%

30

Slightly

anxious

Crystalloid

750-1000

15-30%

>100

Normal

Decreased

Positive

20-30

20-30

Mildly anxious

Crystalloid

1500-2000

20-40%

>120

Decreased

Decreased

Positive

30-40

5-25

Anxious and

confused

Crystalloid

and blood

>2000

>40%

>140

Decreased

Decreased

Positive


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Circulation & Fluid resuscitation

The mainstay of therapy : intravenous fluid

resuscitation

Insert catheter veins : short and large.Central line : time consuming, possibility of

the life threatening complications.

Not give vasopressor (except: cardiogenicshock, cardiac arrest) or bicarbonate


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Hypovolemia should be corrected beforeinduction of anesthesia.

RL less likely to cause hyperchloremic acidosisthan normal saline

In traumatic brain injury avoid RL (RL ishypoosmoler solution , 273 mOsm/lt, NaCl 303mOsm/lt).

Dextrose containing solution may exacerbateischemic brain damage and should be avoidedin the absence of hypoglycemia.


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Hypertonic solution

Colloid

Fluid must be warmed prior to administration.Hypothermia worsens acid-base disorders,

coagulopathies and myocardial function, shift

oxygen-hemoglobin curve to the left, decrease

metabolism lactate, citrate, some anestheticdrugs


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ANESTHESIA

GENERAL

Intravenous

Inhalation

Intramuscular

LOCAL

Topical

Infiltration

Peripheral

nerve block

Spinal

Epidural

Caudal

IVRA

COMBINATION

Spinal +propofol

Caudal+Inhalation


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New trend in GA

Low-flow Anesthesia Low-costAnesthesia

VIMA (Volatile Induction andMaintenance ofAnesthesia)

Fast-Track Anesthesia Single-breath induction (Rapid induction)

SAFE (Short Acting Fast Emergence)


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Choice of anesthesia

In unstable patient base of anesthesia is muscle

relaxant, with general anesthetic agent titrated in

an effort to give amnesia. MAP 50-60 mmHg Patient with mild to moderate degree of

hypovolemia, decrease dose 30-50%

Agitated and uncooperative patient may require

a rapid sequence induction of anesthesiafollowed by laryngoscopy-intubation.


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Anesthetic agent

Ketamine indirectly stimulate cardiac function in

normal patient can display cardiodepresant

properties in shock patients. Avoid N2O : limited oxygen concentration, when

pneumothorax is suspected . Drugs that tend to

lower BP must be avoid

The rate of rise of alveolar concentration ofinhalation anesthetics is greater. Effect of

intravenous anesthetic are exaggerated.


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Variable Halothane Enflurane Isoflurane Sevoflurane

BP

Vascular resistance

Cardiac output

Cardiac contraction

CVP

Heart rate

Sensitization of the

heart to epinephrine

0

0

0

0

0

0?

0

0

0

0

0

Cardiovascular effect of volatile inhalation

anesthetics at 1-1,5 MAC

0 = no change (


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Management of anesthesia

Clear airway

Control ventilation

Avoid increase/decrease of BP

Avoid increase of cerebral vein pressure

Avoid drugs & technique of anesthesia increase ICP.

Nancye Edwards : Principles and Practice of Neuroanaesthesia,1991


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Terimakasih

Tatang Bisri

Bandung, 2004


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Approximate PaO2 versus SpO2

PaO2 SpO2

27 mmHg 50%

30 mmHg 60%

60 mmHg 90%

90 mmHg 100%

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Stabilisasi Resp & Hemidinamik